期刊
CELL DEATH AND DIFFERENTIATION
卷 12, 期 -, 页码 878-892出版社
SPRINGERNATURE
DOI: 10.1038/sj.cdd.4401623
关键词
HIV-1; NeuroAIDS; neurodegeneration; apoptosis; immune activation; macrophages/microglia; neurotoxicity; pharmacology; inflammation; central nervous system
资金
- NCRR NIH HHS [P20 RR15635] Funding Source: Medline
- NEI NIH HHS [R01 EY09024, R01 EY05477] Funding Source: Medline
- NICHD NIH HHS [P01 HD029587] Funding Source: Medline
- NIMH NIH HHS [5P01 MH64570-03] Funding Source: Medline
- NINDS NIH HHS [1P01 NS043985-01, R01 NS050621, 1T32 NS07488, R37 NS36126, R01 NS41207, R01 NS046994, R01 NS 41858] Funding Source: Medline
Infection with the human immunodeficiency virus-1 (HIV-1) can induce severe and debilitating neurological problems that include behavioral abnormalities, motor dysfunction and frank dementia. After infiltrating peripheral immune competent cells, in particular macrophages, HIV-1 provokes a neuropathological response involving all cell types in the brain. HIV-1 also incites activation of chemokine receptors, inflammatory mediators, extracellular matrix-degrading enzymes and glutamate receptor-mediated excitotoxicity, all of which can trigger numerous downstream signaling pathways and disrupt neuronal and glial function. This review will discuss recently uncovered pathologic neuroimmune and degenerative mechanisms contributing to neuronal damage induced by HIV-1 and potential approaches for development of future therapeutic intervention.
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